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<jats:p content-type="fine-print">✓ Tumors of the posterior pituitary are rare and the previous nomenclature has been confusing. A 40-year-old man presented with visual failure and disconnection hyperprolactinemia (830 mU/liter) due to a large invasive pituitary tumor shown to be a pituicytoma (pilocytic astrocytoma). Its astrocytic nature was confirmed by positive immunostaining for glial fibrillary acidic protein and the finding of cytoplasmic filaments on electron microscopy. This case report contains the pathological description of a pituicytoma and illustrates that a non-adenomatous pituitary lesion may masquerade as a pituitary adenoma. Large pituitary lesions associated with serum prolactin concentrations of less than 3000 mU/liter require early surgical biopsy.</jats:p>
OBJECTIVE: Spontaneous intracerebral hemorrhage (ICH) is the commonest form of hemorrhagic stroke and is associated with a poor prognosis. Neurosurgical removal of intracerebral hematoma has limited benefit and no pharmacotherapies are available. In acute ICH, primary tissue damage is followed by secondary pathology, where the cellular and neuroinflammatory changes are poorly understood. METHODS: We studied histological changes in postmortem tissue from a cohort of spontaneous supra-tentorial primary ICH cases (n = 27) with survival of 1-12 days, compared to a matched control group (n = 16) examined in corresponding regions. Hematoxylin-eosin and microglial (Iba1) immunolabelled sections were assessed at 0-2, 3-5, and 7-12 days post-ICH. RESULTS: Peri-hematoma, the observed ICH-related changes include edema, tissue neutrophils and macrophages from day 1. Ischemic neurons and swollen endothelial cells were common at day 1 and universal after day 5, as were intramural erythrocytes within small vessel walls. Activated microglia were evident at day 1 post-ICH. There was a significant increase in Iba1 positive area fraction at 0-2 (threefold), 3-5 (fourfold), and 7-12 days post ICH (ninefold) relative to controls. Giant microglia were detected peri-hematoma from day 5 and consistently 7-12 days post-ICH. INTERPRETATION: Our data indicate that neuroinflammatory processes commence from day 1 post-ICH with changing microglial size and morphology following ICH and up to day 12. From day 5 some microglia exhibit a novel multiply nucleated morphology, which may be related to changing phagocytic function. Understanding the time course of neuroinflammatory changes, post-ICH may reveal novel targets for therapy and brain restoration.
Presynaptic serotonergic markers in community-acquired cases of Alzheimer's disease: correlations with depression and neuroleptic medication.
Presynaptic serotonergic markers, serotonin uptake sites, and concentrations of serotonin and 5-hydroxyindoleacetic acid were studied in the frontal and temporal cortex of 20 community-acquired cases of Alzheimer's disease and 16 controls matched for age, sex, postmortem delay, and storage. Clinical assessments, including behavioural symptoms, of the Alzheimer patients were made at 4-month intervals during life. There was significant reduction in the number of serotonin uptake sites in Alzheimer cases in temporal but not frontal cortex. There was no significant alteration in the concentrations of serotonin or 5-hydroxyindoleacetic acid in either region. Alzheimer patients who had persistent depressive symptoms during life had significantly fewer serotonin uptake sites in both cortical areas compared with Alzheimer patients without these symptoms. In addition, Alzheimer patients who were receiving chronic neuroleptic medication had significantly lower concentrations of serotonin in frontal cortex and 5-hydroxyindoleacetic acid in temporal cortex than those patients not receiving such treatment. These data suggest previous studies that reported uniform serotonergic dysfunction may have been subject to unintentional selection of behaviourally disturbed Alzheimer cases or those receiving chronic neuroleptic medication. This study also provides a basis for the treatment of behaviourally disturbed Alzheimer patients with serotonomimetics.